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Page 286 Schwarzenbach et al. Cancer Drug Resist 2019;2:271-96 I http://dx.doi.org/10.20517/cdr.2019.010

miR-148b-5p Down- n.d. [141]
miR-141, Down-/up- n.d. [186]
miR-200,
miR-429
miR-484 DOwn- VEGF B, VEGF receptor 2 [187]
Cis- and carboplatin resistance
miR-21,
miR-181a,
miR-223, Down-/up- n.d. [143]
miR-486,
miR-1908
miR-622 Up- Ku complex [146]
ABCC2: adenosine triphosphate-binding cassette subfamily C member 2; ABCC5: ATP-binding cassette subfamily C member 5; ALK7:
activin receptor-like kinase 7; BAK1: Bcl-2 antagonist killer 1; BCL2: B-cell lymphoma-2; BCL2L2: BCL2 like 2; BIRC3: baculoviral IAP
repeat-containing 3; CDK1: cyclin-dependent kinase 1; CCNA1/CCND1: cyclin A1/D1 gene; CSF-1: colony-stimulating factor 1; DAPK2:
death-associated protein kinase 2; DDR1: Discoidin Domain Receptor 1; DNMT: DNA methyltransferase; EGFR: epithelial growth factor
receptor; ERCC1: excision repair cross-complementation group 1; ERK1: extracellular signal-regulated kinase 1; EZH2, enhancer of zeste
homolog 2; FOXO3: forkhead box O3; GRB2: growth factor receptor-bound protein 2; GST-π: glutathione S-transferase π; GOLPH3:
Golgi phosphoprotein-3; IAP2: inhibitor of apoptosis protein-2; IGF2BP1: insulin-like growth factor 2 mRNA-binding protein 1; INPPL1:
inositol polyphosphate phosphatase-like 1; ITGB8: integrin subunit beta 8; KEAP1: Kelch-like erythroid-derived cap-n-collar homology-
(ECH-) associated protein-1; KCNMA1: potassium channel calcium activated large conductance subfamily M alpha, member 1; MFAG:
musculoaponeurotic fibrosarcoma oncogene family, protein G; MCL1: myeloid cell leukemia sequence 1; MDR1: multidrug resistance 1;
MET: mesenchymal-epithelial transition factor; MST1: STE20-like kinase; PDCD4: programmed cell death 4; PTEN: phosphatase and
tensin homolog; mTOR: mammalian target of rapamycin; NAV3: neuron navigator; RB1: retinoblastoma 1; RSK2: ribosomal protein S6
kinase; S100A7: S100 calcium-binding protein A7; SAV1: salvador homolog 1; SHC1: Src Homology 2 Domain Containing 1; TRIM31: ring
finger, B-box and coiled-coil domain protein, tripartite motif; VEGF: vascular epithelial growth factor; WLS: wntless (Wnt) ligand secretion
mediator; XIAP: X-linked inhibitor of apoptosis; ZEB1: zinc finger E-box binding homeobox 1; n.d.: not determined

rate. In addition, the expression levels of P-glycoprotein involved in multi-drug resistance (MDR) decreased
with increasing cisplatin concentrations.

Using microarrays and RNA-sequencing, Samuel et al. assessed the role of miR-31 in the development of
[114]
chemo-resistance to cisplatin. They found increased levels of miR-31 and reduced levels of potassium channel
calcium activated large conductance subfamily M alpha, member 1 (KCNMA1), a subunit of calcium-regulated
big potassium (BK) channels in resistant ovarian cells. Overexpression of miR-31, knockdown of KCNMA1
or inhibition of BK channels increased resistance to cisplatin, suggesting that this resistance was mediated
by the repression of KCNMA1 through miR-31.

Recently, Lv et al. showed that the overexpression of HDAC1 decreased cisplatin sensitivity, promoted
[115]
proliferation and blocked the suppressive effects of miR-34a on cell proliferation in ovarian cancer cells.
Accordingly, miR-34a directly bound to HDAC1, and downregulated its expression, which subsequently
decreased the resistance to cisplatin and suppressed proliferation in ovarian cancer cells.

In both epithelial ovarian cancer cell lines and ovarian carcinomas, Li et al. analyzed the expression
[116]
of miR-128 and its targeted genes, the polycomb ring finger oncogene Bmi-1 and the ATP-binding cassette
subfamily C member 5 (ABCC5). MiR-128 expression was significantly reduced in the cisplatin-resistant
ovarian cancer cell line compared with its parental SKOV3 cells, and decreased upon treatment with cisplatin
in a concentration-dependent manner. Overexpression of miR-128 re-sensitized the cells to cisplatin and
reduced the expression of cisplatin-resistant-related proteins ABCC5 and Bmi-1. Administration of a
combination of cisplatin and miR-128 inhibited the growth of cisplatin resistant xenograft tumors more
effectively than cisplatin alone.

Investigating the role of miR-130b in the development of multidrug-resistance, Yang et al. detected that
[117]
down-regulation of miR-130b in ovarian cancer correlated with FIGO III-IV clinical stages, poor histological